Virus-Induced Thyroiditis

Srinivasappa, Javaraiah; Garzelli, Carlo; Onodera, Takashi; Ray, Usharanjan; Notkins, Abner Louis

doi:10.1210/endo-122-2-563

Cited by 35 publications

(18 citation statements)

References 9 publications

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“…Mice infected with reovirus type 1 develop IgM antibodies to thyroglobulin within 1 wk; subsequently IgG antibodies can be detected. Three to four weeks after infection, up to 75% of the animals showed evidence of focal thyroiditis, characterized by irregular small necrotic areas in the follicles with leukocytic infiltration and a decrease in colloid (24).…”

Section: Discussionmentioning

confidence: 99%

Association of Parvovirus B19 Infection and Hashimoto's Thyroiditis in Children

et al. 2008

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Hashimoto's thyroiditis is a common autoimmune disorder of the thyroid gland. It has been linked to infections with hepatitis C, EBV, HTLV-1, and Yersinia enterocolitica. As parvovirus B19 has been associated with a wide spectrum of autoimmune diseases, we investigated the potential role of B19 infection in inducing Hashimoto's thyroiditis. Serum samples derived from 73 children and adolescents with Hashimoto's thyroiditis and from 73 age-matched controls were included in the study. The mean age of disease manifestation was 10 y 7 mo. All samples were analyzed for the presence of viral DNA and for antibodies against VP1, VP2, and NS1 proteins. VP1- and VP2-specific antibodies were present in 38 patients (52%) and 43 controls (59%; N.S.). NS1-specific antibodies were detectable in 23 patients (32%) and 19 controls (26%; N.S.). Parvovirus B19 DNA was detectable in 9 patients (12%) and 2 controls (3%; p < 0.03), indicating recent B19-infection. A negative correlation between disease duration and the detection of viral DNA was seen. The mean disease duration in B19-DNA-positive patients was 6 mo, compared to 29 mo in the remainder (p < 0.01). There is strong evidence that acute parvovirus B19 infections are involved in the pathogenesis of some cases of Hashimoto's thyroiditis.

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Section: Discussionmentioning

confidence: 99%

Association of Parvovirus B19 Infection and Hashimoto's Thyroiditis in Children

et al. 2008

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“…Non-dominant Tg peptides may contribute toward pathogenesis within the context of two main theories of thyroiditis induction; namely, Tg iodination (Sundick et al 1987) and infection (Srinivasappa et al 1988). Compelling evidence (Champion et al 1987;Champion et al 1992, Sundick et al 1987Champion et al 1991) suggests that iodination enhances Tg immunogenicity, but it is not yet clear whether this enhancement results solely from the creation of dominant (and/or) iodinated T-cell epitopes or involves novel (non-dominant?)…”

Section: Discussionmentioning

confidence: 99%

“…Our earlier (Chronopoulou and Carayanniotis 1992;Chronopoulou and Carayanniotis 1993) and present results, and other studies (Texier et al 1992), clearly demonstrate that Tg determinants do not need to be iodinated in order to cause EAT. In the context of infection, non-dominant Tg peptides may be recognized via molecular mimicry with proteins from various pathogens, such as the reovirus, that causes mouse thyroiditis (Srinivasappa et al 1988) and induces class II MHC expression on thyroid cells (Neufeld et al 1989). They may also cross-react with proteins from microbial flora that predispose for thyroiditis (Penhale and Young 1988).…”

Section: Discussionmentioning

confidence: 99%

Distinct genetic pattern of mouse susceptibility to thyroiditis induced by a novel thyroglobulin peptide

1994

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Experimental autoimmune thyroiditis (EAT), induced by thyroglobulin (Tg) and adjuvant, is major histocompatibility complex-controlled and dependent on Tg-reactive T cells, but the immunopathogenic T-cell epitopes on Tg remain mostly undefined. We report here the thyroiditogenicity of a novel rat Tg peptide (TgP2; corresponding to human Tg amino acids 2695-2713), identified by algorithms as a site of putative T-cell epitope(s). TgP2 causes EAT in SJL (H-2s) but not in C3H or B10.BR (H-2k), BALB/c (H-2d), and B10 (H-2b) mice. This reveals a new genetic pattern of EAT susceptibility, since H-2k mice are known to be high responders (susceptible) after Tg challenge. Following in vivo priming with TgP2, T cells from only SJL mice proliferated significantly and consistently to TgP2 in vitro, whereas TgP2-specific IgG was observed in all strains tested. Adoptive transfer of TgP2-primed SJL lymph node cells to naive syngeneic recipients induced a pronounced mononuclear infiltration of the thyroid, which was more extensive than that observed after direct peptide challenge. TgP2 is non-immunodominant, since priming of SJL mice with rTg did not consistently elicit T-cell responses to TgP2 in vitro and a TgP2-specific T-cell hybridoma did not respond to antigen presenting cells pulsed with rTg. The data support the notion that Tg epitopes need not be either iodinated or immunodominant in order to cause severe thyroiditis and that the genetic pattern of the disease they induce can be distinct from that of Tg-mediated EAT.

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“…Other known pathogenic Tg peptides either do not behave similarly [7,10], or have not been tested for the above parameters [II]. Autoreactive B cells might be triggered against non-dominant Tg pcptides such as TgPI by cross-reactive epitopes from bacteria [12] or viruses [13,14] linked to thyroid pathogenesis, although direct evidence for such events is still lacking. Once elicited, these autoantibodies may play a role in the initiation or amplification of the disease cascade via mechanisms such as antibody-dependent cell-mediated cytotoxicity (ADCC) i 15] or immune complex deposition [ 16], that have been suggested to participate in the disease process.…”

Section: Discussionmentioning

confidence: 99%

Autoreactive IgG elicited in mice by the non-dominant but pathogenic thyroglobulin peptide (2495–2511): implications for thyroid autoimmunty

Chronopoulou

Michalak

Carayanniotis

1994

Clinical and Experimental Immunology

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SUMMARYWe have previously shown that mice challenged with the rat thyroglobulin (Tg) peptide TgPI (corresponding to aa 2495-2511 of human Tg) develop experimental autoimmune thyroiditis (EAT) and produce IgG antibodies that cross-react with Tg from various species. It was not clear, however, whether such antibodies were TgPl-specific or were induced secondarily-i.e. by autologous Tg released from the destroyed gland-and therefore directed to determinants other than TgPl, In this study we describe ihat, 5 weeks after priming with TgPI. the binding of serum IgG on native Tg is completely inhibited by free peptide, suggesting lack of recognition of other determinants on mouse Tg (mTg), In addition, TgPt-induced but not mTg-induced IgG bound better to heat-denatured than intact mTg, a result compatible with the recognition of a linear epitope by the peptide-induced antibodies. Comparison of the IgG subclass distribution among mTg-induced versus TgPl-induced IgG did not reveal qualitative differences, since all subclasses were represented in the order IgGl > IgG2b > IgG2a > IgG3. Finally, TgPl-specific IgG reacted strongly with the foUicular colloid in sections of normal thyroids, indicating the potential to bind to native Tg in vivo. These data: (i) highlight TgPl as the only, so far, Tg sequence known to generate both EAT and Tg-reactive IgG in mice: and (ii) do not provide evidence for an amplification of the Tg-specific IgG response through the involvement of endogenous autoanligen in EAT.

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Virus-Induced Thyroiditis

Cited by 35 publications

References 9 publications

Association of Parvovirus B19 Infection and Hashimoto's Thyroiditis in Children

Association of Parvovirus B19 Infection and Hashimoto's Thyroiditis in Children

Distinct genetic pattern of mouse susceptibility to thyroiditis induced by a novel thyroglobulin peptide

Autoreactive IgG elicited in mice by the non-dominant but pathogenic thyroglobulin peptide (2495–2511): implications for thyroid autoimmunty

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